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Y3- I & W > Heart disorders > Flashcards

Heart disorders Flashcards

we will cover normal heart function ischaemic heart function MI heart failure valvular heart disease

1
Q

describe normal heart anatomy

A

there are 2 atrium 2 ventricles

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2
Q

what valve lies in between the left atrium and left ventricle

A

the mitral valve/ bi CUSPID

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3
Q

how does blood travel around the heart

A

deoxygenated blood enters the Vena cava into the right atrium the tricuspid valve opens and blood moves into the RV after the SL valve opens and blood is carried into the pulmonary artery to get oxygen oxygenated blood is passed into the LA and then LV into the aorta to flow around the body

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4
Q

what is diastole

A

the filling of the ventricles when the heart is relaxed

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5
Q

what is systole

A

when the heart is contracting forcing blood out of the ventricles

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6
Q

what are the three main vessels that supply oxygenated blood directly to the heart

A

right coronary artery left anterior descending artery circumflex artery

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7
Q

what are the branches of the left main coronary artery

A

the circumflex artery left anterior descending artery

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8
Q

where does the left main coronary artery branch from

A

the aorta

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9
Q

definition of ischaemic heart disease

A

a group of clinical syndromes( signs and symptoms) that relate to myocardial ischaemia

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10
Q

definiton of ischaemia

A

is cell injury resulting from hypoxia induced by reduced blood flow most commonly due to a mechanical arterial obstruction

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11
Q

how many people die of ischaemia per year

A

64000

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12
Q

what are the clinical manifesations of ischaemic heart disease

A

MI

angina

chronic ischaemic heart disease

sudden cardiac death

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13
Q

why have death rates fallen by ischameic heart disease

A

due to awareness/prevention

and diagnosis and treatment

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14
Q

what can people to to prevent ischaemic heart disease

A

diet and exercise and modifiable risk factors such as hypertension and diabetes

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15
Q

what medications can people use to lower cholesterol

A

statins

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16
Q

what treatment can people undergo to reduce the likelihood of death by ischaemic heart disease

A

drugs- statins

acute presentations- antioplasty, stenting etc

arrythmias- implantable defib

heart failure- ventricular assist devices

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17
Q

what are the risk factors of ischamic heart disease

A

smoking

obesity

hypertension

diabetes

age

dsylipidaemia

family history

higher risk in men > woman

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18
Q

what is dyslipidaemia

A

due to increased levels of LDL in the blood

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19
Q

how do we treat dyslipidaemia

A

with the use of statins

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20
Q

what is the pathogenesis of ischaemic heart disease

A

insufficient coronary perfusion –> cardiac hypoxia –> cell injury which is sustained –> myocardial cell death leading to MI

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21
Q

describe LAD obstruction

A

sudden death artery AKA widowmaker

anterior infartion

50% of cases

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22
Q

descirbe circumflex obstruction

A

lateral infarction

20% of cases

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23
Q

describe right coronary artery obstruction

A

interior infarction

30% of cases

can involve the posterior septum

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24
Q

what can happen in ischamic heart disease on a cellular level

A

can lead to a reduction in oxidative phosphrylation and therefore reduction of ATP

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25
Q

As ATP levels falls what three pathways can occur

A
  1. reduction in the Na+ pump
  2. increase in anaerobic respiation
  3. dettatchment of ribosomes
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26
Q

what happens when there is a reduction in the sodium pump

A

leads to influx of ca2+, H20 and Na+

efflux of K+

leading to endoplasmic reticulum swelling and loss of microvilli

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27
Q

what does an increase of anaerobic respiration lead to

A

decreased glycogen

increased lactic acid therefore low pH

clumping together of nuclear chromatin

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28
Q

what happens in ribosomes dettach

A

leading to decrease in protein synethesis

29
Q

explain the three pathways that occur when there is reduction in oxidative phosphorylation in the cellular level of ischaemic heart disease

A
30
Q

what is artherosclerosis

A

material build up in the arterial wall due to fatty deposits

31
Q

what are risk factors for artherosclerosis

A

smoking and BP

32
Q

what else is located near the artherosclerosis

A

macrophaged which can initiate an inflammatory response

33
Q

what does the pre clinical phase include of atherosclerosis

A

normal artery leads to fatty streak –> fibrofatty plaque –> advanced vunerable plaque

34
Q

what does the clinical phase of artherosclerosis include

A

aneurysm and rupture

occlusion by thrombus

critical stenosis

35
Q

what are unstable angina and MI caused by

A

plaque rupture

36
Q

what is the difference between angina and MI

A

there is no detectable cell damage in angina

37
Q

what are the clinical features of angina pectoris

A

strangled chest

pain due to inflammatory mediator

pain can be behind restrosternal chest pain, radiationto the epigastric shoulders

precipitated by running, eating, exposure to cold or stress

38
Q

what is stable angina

A

1-5 minutes relieved by GTN spray

39
Q

what are the characterisrics of unstable angina

A

intense

lasts longer

less exertion

spontaneous at rest

progressive pain

40
Q

what are symrpoms of unstable angina

A

pale and clammy

sweating

weak pulse

nausea and vomitting

breathlessness

41
Q

how do we diagnose ischamic heart disease

A

clinical features- severity of pain

changes on ECG

cardia blood markers

42
Q

what is the theory of seeing cardiac blood markers in the blood

A

proteins such as troponin are normally held in cardiomyocytes –> released when the myocyte is necrotic and released into the blood stream

43
Q

what do we do if GTN spray doesnt work

A

Call 999

Reassure/comfortable position

Give oxygen

Sublingual GTN

No Intra muscular injections! As they are too slow, and risk of bleeding

Give aspirin 300mg- provide note for hospital admin

If pt is unconscious begin resuscitation

44
Q

what about non symptomatic ischaemic heart disease pts

A

patients are vunerable for upto 4+ weeks following MI or sudden increase in angina symptoms

45
Q
A
46
Q

what do we not recommend for patients who had coronary artery bypass graft

A

antibiotic prophylaxis

47
Q

what are complications of an MI

A

Impaired contractility

tissue necrosis

electrical instability

pericardial inflammation

48
Q

6 results

what can be the issues with MI

A

stroke

cardiogenic shock

congenetive HF

cardiac tamponade

arrythmias

pericarditis

49
Q

what is HF

A

an inability to pulp enough blood to meet metabolic demands of the body

50
Q

symptoms of HF

A

fatigue

breathless ness

peripheral oedema

51
Q

which mechanisms help the failing heart maintain function

A

increase contractility

cardiac hypertrophy

neurohumoral responses

52
Q

describe neurohumoral responses

A

fluid overload

fluid retention to maintain

renin angiotensin system

low cardiac output

53
Q

what is cardiac hypertropy characterised by

A

increased heart size and mass

increased protein synthesis

fibrosis

abnormal proteins

54
Q

what is the ejection fraction

A

the proportion of the blood that is actually ejected from the ventricles

55
Q

what is systolic dysfuction

A

decreased contraxctility and therefore the ejection function decreeases to less than <40%

heart failure with reduced ejection function HRrEF

56
Q

what is the typical ejection fraction

A

55-70%

57
Q

what do we DIASTOLIC dysfunction

A

heart cannot fill proeprly with blood

heart failure with preserved ejection fracture HFpEF

58
Q

describe left heart failure

A

damage to the left ventricles or valve

can lead to

Congestion in the pulmonary circulation, stasis of blood in the LS and inadequate perfusion of organs

59
Q

what are the symptoms of Left heart disease

A

Breathlessness

Oedema due to pulmonary congestion

systemic hypoperfusion (organ failure

60
Q

describe right heart failure

A

Increased back pressure through the pulmonary and venous circulation

Therefore leg swells

Most people have a combination of both

61
Q

how do people get right heart failure

A

from left heart failure or pulmonary issues

62
Q

what are the different types of valvular heart diseases

A

fail to fully open eg stenosis

fail to fully close eg flow reversal

vegetations - infective nodules the formation of infective vegetations on the heart is called infective endocarditis

63
Q

what does abnormal valve function

A

abnormal blood flow

clot formation

risk of infection

64
Q

what is stenosis due to

A

chronic injury / rheumatic fever

65
Q

what is the pathological cause of mitral stenosis

A

rheumatic valvular disease

66
Q

what can left ventricular hypertrophy lead to

A

ischaemia

syncope

decompensated Congenitive heart failure

67
Q

why can we get mitral regurgitation

A

Calcification of the valve ring

Fibrous scarring of the papillary muscle and tethering valve leaflets

The papillary muscle can also rupture

Infective endocarditis

68
Q

how can we fix mitral regurgitation

A

valve replacement

69
Q
A

Y3- I & W (21 decks)

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